title: How to live long and prosper: autophagy, mitochondria, and aging.
abstract: Autophagy is a process of cellular self-degradation in which portions of the cytoplasm are sequestered within cytosolic double-membrane vesicles and delivered to the lysosome/vacuole. This process occurs in all eukaryotic cells and is partly a stress response; autophagy is induced during starvation and hypoxia. However, autophagy also plays a role during development and is associated with a range of diseases. Accumulating data also suggest the involvement of autophagy in aging. For example, the role of various hormones and nutrient sensing pathways in life span extension may involve autophagy. Similarly, autophagy is the primary mechanism for removing damaged organelles, such as mitochondria, which may have a direct impact on aging. Here, we review the role of autophagy, with an emphasis on the signaling pathways that are involved in regulation, and the consequences of autophagy induction with regard to aging.
authors.affiliation: Life Sciences Institute, and Departments of Molecular, Cellular, and Developmental Biology, and Biological Chemistry, University of Michigan, Ann Arbor, Michigan, USA.
authors.forename: Wei-Lien
authors.initials: WL
authors.lastname: Yen
authors.forename: Daniel J
authors.initials: DJ
authors.lastname: Klionsky
mesh_terms: D000375:Aging / Q000502:physiology*; D000818:Animals; D001343:Autophagy / Q000502:physiology*; D031204:Caloric Restriction; D006801:Humans; D008928:Mitochondria / Q000502:physiology*; D017382:Reactive Oxygen Species / Q000378:metabolism; D015398:Signal Transduction / Q000502:physiology
chemical_list: D017382:Reactive Oxygen Species